Misonidazole (MISO) is a bioreductively-activated marker of cellular hyposiz which preferentially binds to cells with decreased oxygen content. Research using MISO experimentally in rats has been divided into three phases. In phase I, tritiated MISO retention in rat dental pulp was determined using liquid scintillation counting. Comparisons were made between normoxia (normal oxygen tension) and induced hypobaric hypoxia. Induced hypoxiz significantly increased MISO retention over the normoxic condition. In phase II, the localization of tritiated MISO in normoxic and hypoxic states were determined through use of autoradiography. Increased MISO retention in the induced hypoxic animals was via two mechanisms: (1) an overall increased retention due to a uniform reduction of the oxygen supply to the tissues, and (2) a site-specific increase in hypoxic retention due to either poor oxygen diffusion (in cementoblasts) or to capillary shutdown (pulp horn odontoblasts). Phase III is underway in which the effects of experimentally induced pulpal inflammation (using cavity preparation) on MISO retention will be studied. This may shed light on pulpal oxygen perfusion status at times of operative stress that is normally produced in clinical situations.